Pathogenesis of airway hyperreactivity.
Chest 1988 Jun; 93(6):1278-1280
Current scientific opinions and data concerning airway hyperreactivity and the mechanisms causing this to occur were reviewed and discussed. The review focused on information which may offer insight into the mechanisms by which airway injury results in acute airway hyperreactivity. Investigators have studied acute experimental airway disorders in animals characterized, at least in part, by hyperreactivity. At the start of hyperreactivity there appears to be no increase in inflammatory cells, but this rapidly changes. Rather than being a cause of airway hyperreactivity, however, neutrophilic infiltration of the airways appears as a consequence of the acute, nonimmunologic airway injury producing the hyperreactivity. The hypothesis that neutrophilic infiltration causes the acute increase in airway reactivity during an asthma attack is flawed by the finding that such attacks are associated with airway eosinophilic and not neutrophilic infiltration and exudation. The author suggests that the early onset increase in reactivity after immunologic airway injury is related to the generation by normal lung cell constituents of mediators that increase reactivity status. The author suggests that the cellular events causing hyperreactivity do so by increasing airway neuromuscular responsiveness and not by producing tissue inflammatory cell infiltration or edema. Several possible mechanisms for the potentiation of one bronchoconstrictor's effect by another at airway neuromuscular junctions were presented.
NIOSH-Publication; NIOSH-Grant; Pulmonary-system-disorders; Lung-function; Pulmonary-function; Bronchial-asthma
Internal Medicine Univ of Tennessee, Memphis 956 Court Avenue Memphis, TN 38163
University of Cincinnati, Cincinnati, Ohio